Parathyroid hormone

Parathyroid hormone is the most important endocrine regulator of calcium

and phosphorus concentration in extracellular fluid
major target cells in bone and kidney

Physiologic Effects of Parathyroid Hormone

o Mobilization of calcium from bone: stimulate osteoclasts to reabsorb bone
mineral, liberating calcium into blood.
o Enhancing absorption of calcium from the small intestine:

Facilitating calcium absorption from the small intestine to elevate blood

levels of calcium.

Parathyroid hormone stimulates this process, but indirectly by stimulating

production of the active form of vitamin D in the kidney.

Vitamin D induces synthesis of a calcium-binding protein in intestinal

epithelial cells that facilitates efficient absorption of calcium into blood.

o Suppression of calcium loss in urine: puts a brake on excretion of calcium in

urine, thus conserving calcium in blood. This effect is mediated by stimulating
tubular reabsorption of calcium. Another effect of parathyroid hormone on the
kidney is to stimulate loss of phosphate ions in urine.

Regulation

Parathyroid hormone is released in response to low extracellular

concentrations of free calcium

Disease state

Excessive secretion of parathyroid hormone is seen in two forms:

Primary hyperparathyroidism is the result of parathyroid gland disease, most commonly

due to a parathyroid tumor (adenoma) which secretes the hormone without proper
regulation. Common manifestations of this disorder are
o chronic elevations of blood calcium concentration (hypercalcemia),
o

kidney stones

Decalcification of bone.

Secondary hyperparathyroidism is the situation where disease outside of the parathyroid

gland leads to excessive secretion of parathyroid hormone. A common cause of this
disorder is kidney disease - if the kidneys are unable to reabsorb calcium, blood calcium
levels will fall, stimulating continual secretion of parathyroid hormone to maintain
normal calcium levels in blood. Secondary hyperparathyroidism can also result from
inadequate nutrition - for example, diets that are deficient in calcium or vitamin D, or
which contain excessive phosphorus (e.g. all meat diets for carnivores). A prominent
effect of secondary hyperparathyroidism is
o

decalcification of bone, leading to pathologic fractures or "rubber bones".

symptoms of hyperparathyroidism

moans" (complaints of not feeling well)

"groans" (abdominal pain, GERD)
"stones" (kidney)
"bones" (bone pain)
"psychiatric overtones" (lethargy, fatigue, depression, memory problems)

Diagnosis

blood levels of calcium and parathyroid hormone are too high

o increased bone resorption, allowing flow of calcium from bone to blood

o reduced renal clearance of calcium
o increased intestinal calcium absorption

serum phosphorus levels are abnormally low as a result of decreased renal

tubular phosphorus reabsorption. This contrasts with secondary
hyperparathyroidism, in which serum phosphorus levels are generally
elevated because of renal disease.

TREATMENT
surgical removal

Calcimimetics are a new class of drug that turns off secretion of PTH

Hypoparathyroidism

inadequate production of parathyroid hormone

decreased concentrations of calcium and increased concentrations of
phosphorus in blood
Common causes of this disorder include surgical removal of the parathyroid
glands and disease processes that lead to destruction of parathyroid glands
Hypocalcemia -leads to tetany and convulsions, and can be acutely lifethreatening
Symptom

o Tingling in the lips, fingers, and toes

o Dry hair, brittle nails, and dry, coarse skin
o Muscle cramps and pain in the face, hands, legs, and feet
o Cataracts on the eyes
o Malformations of the teeth, including weakened tooth enamel and misshapen
roots of the teeth
o Loss of memory
o Headaches
o Severe muscle spasms (also called tetany) and convulsions
Treatment

Restore body calcium and phosphate to normal level

o central venous catheter is recommended, as the calcium can
irritate peripheral veins and cause phlebitis